We did not find evidence that SPCD is qualitatively distinct from ASD. Rather, it appears to lie on the borderlands of the autism spectrum, describing those with autistic traits that fall just below the threshold for an ASD diagnosis. SPCD may have clinical utility for identifying people with autistic traits that are insufficiently severe for ASD diagnosis, but who nevertheless require support.

RationaleReversal learning requires associative learning and executive functioning to suppress non-adaptive responding. Reversal-learning deficits are observed in e.g. schizophrenia and obsessive-compulsive disorder and implicate neural circuitry including the orbitofrontal cortex (OFC). Serotonergic function has been strongly linked to visual reversal learning in humans and experimental animals but less is known about which receptor subtypes are involved.ObjectivesThe objectives of the study were to test the effects of systemic and intra-OFC 5-HT2C-receptor antagonism on visual reversal learning in rats and assess the psychological mechanisms underlying these effects within novel touchscreen paradigms.MethodsIn experiments 1–2, we used a novel 3-stimulus task to investigate the effects of 5-HT2C-receptor antagonism through SB 242084 (0.1, 0.5 and 1.0 mg/kg i.p.) cross-site. Experiment 3 assessed the effects of SB 242084 in 2-choice reversal learning. In experiment 4, we validated a novel touchscreen serial visual reversal task suitable for neuropharmacological microinfusions by baclofen-/muscimol-induced OFC inactivation. In experiment 5, we tested the effect of intra-OFC SB 242084 (1.0 or 3.0 μg/side) on performance in this task.ResultsIn experiments 1–3, SB 242084 reduced early errors but increased late errors to criterion. In experiment 5, intra-OFC SB 242084 reduced early errors without increasing late errors in a reversal paradigm validated as OFC dependent (experiment 4).ConclusionIntra-OFC 5-HT2C-receptor antagonism decreases perseveration in novel touchscreen reversal-learning paradigms for the rat. Systemic 5-HT2C-receptor antagonism additionally impairs late learning—a robust effect observed cross-site and potentially linked to impulsivity. These conclusions are discussed in terms of neural mechanisms underlying reversal learning and their relevance to psychiatric disorders.Electronic supplementary materialThe online version of this article (doi:10.1007/s00213-015-3963-5) contains supplementary material, which is available to authorized users.

Antiretroviral therapy (ART) limits human immunodeficiency virus 1 (HIV-1) replication but does not eliminate the long-lived reservoir established shortly after viral acquisition. A successful HIV cure intervention necessitates either elimination or generation of long-term immune control of the persistent viral reservoir. Immune modulating strategies in conjunction with ART hold promise for achieving cure by inducing viral antigen expression and augmenting infected cell killing.

Interventions rarely have a universal effect on all individuals. Reasons ranging from participant characteristics, context and fidelity of intervention completion could cause some people to respond more positively than others. Understanding these individual differences in intervention response may provide clues to the mechanisms behind the intervention, as well as inform future designs to make interventions maximally beneficial for all. Here we focus on an intervention designed to improve adolescent wellbeing, and explore potential moderators using a representative and well-powered sample. 16-year old participants (N = 932) in the Twins Wellbeing Intervention Study logged online once a week to complete control and wellbeing-enhancing activities consecutively. Throughout the study participants also provided information about a range of potential moderators of intervention response including demographics, seasonality, personality, baseline characteristics, activity fit, and effort. As expected, some individuals gained more from the intervention than others; we used multi-level modelling to test for moderation effects that could explain these individual differences. Of the 15 moderators tested, none significantly explained individual differences in intervention response in the intervention and follow-up phases. Self-reported effort and baseline positive affect had a notable effect in moderating response in the control phase, during which there was no overall improvement in wellbeing and mental health. Our results did not replicate the moderation effects that have been suggested by previous literature and future work needs to reconcile these differences. They also show that factors that have previously been shown to influence baseline wellbeing do not also influence an individual’s ability to benefit from a wellbeing intervention. Although future research should continue to explore potential moderators of intervention efficacy, our results suggest that the beneficial effect of positive activities in adolescents were universal across such factors as sex and socioeconomic status, bolstering claims of the scalability of positive activities to increase adolescent wellbeing.

Behavioral traits generally show moderate to strong genetic influence, with heritability estimates of around 50%. Some recent research has suggested that trust may be an exception because it is more strongly influenced by social interactions. In a sample of over 7,000 adolescent twins from the United Kingdom’s Twins Early Development Study, we found broad sense heritability estimates of 57% for generalized trust and 51% for trust in friends. Genomic-relatedness-matrix restricted maximum likelihood (GREML) estimates in the same sample indicate that 21% of the narrow sense genetic variance can be explained by common single nucleotide polymorphisms for generalized trust and 43% for trust in friends. As expected, this implies a large amount of unexplained heritability, although power is low for estimating DNA-based heritability. The missing heritability may be accounted for by interactions between DNA and the social environment during development or via gene–environment correlations with rare variants. How these genes and environments correlate seem especially important for the development of trust.